1. Field of the Invention
This invention pertains to ventricular pacing. More particularly, this invention pertains to synchronous pacing of a patient's left ventricle by electrodes residing in the patient's right ventricle.
2. Description of the Prior Art
a. Pacing for Bradycardia
Percutaneously placed pacing electrodes are commonly positioned only in the right-side chambers (right atrium or right ventricle) of the heart. Access to such chambers is readily available. Such access is through the superior vena cavity into the right atrium and then into the right ventricle.
Electrode placement into the left ventricle is normally avoided. Access is not as direct as in right ventricle placement. More important, emboli risk in the left ventricle is greater than in the right ventricle. Emboli which might develop in the left ventricle by reason of the electrode placement have direct access to the brain via the aorta from the left ventricle. This presents a significant risk of stroke.
Historically, pacing electrodes were placed only in the right ventricle to treat bradycardia (slow heart rate). Right atrium pacing was less understood and was more complex.
With advances in electro-physiology, pacing of both the right atrium and right ventricle was developed. Such dual chamber pacing resulted in better hemodynamic output than right ventricle-only pacing.
In addition to treating bradycardia, dual chamber pacing maintained synchrony between the chambers. Recent clinical evidence suggests that conventional ventricular pacing from the right ventricle creates asynchronous contraction of the left ventricle, leading to inefficient mechanical contraction and reduced hemodynamic performance. Long term right ventricular pacing has even been found to be associated with an increased risk of developing or worsening heart failure.
At first, combined pacing of the right ventricle and right atrium was performed by advancing two electrode leads through the superior vena cava into the right atrium. The first of these terminated at one or more electrodes which were attached to the endocardium of the atrium. The second lead (also having one or more electrodes) was advanced into the right ventricle with the electrode attached to the endocardium of the right ventricle.
Such historical dual chamber pacing was not without complications. The use of two leads resulting in a doubling of volume of the vasculature (e.g., the superior vena cava and jugular vein) occupied by such leads. Further, attachment of an electrode to the atrial wall was unreliable.
The historical problems of the dual chamber pacing led to the development of so-called “single pass” leads. Such leads have both the atrial and ventricle electrodes on a common lead.
An example of a single pass lead for pacing both the right ventricle and right atrial is taught in U.S. Pat. No. 6,230,061 B1 to Hartung issued May 8, 2001. The lead of the '061 patent is described as floating lead in that the lead and electrodes are not attached to the walls of the heart. In one embodiment of the '061 patent (FIG. 4a), two electrodes in the right atrium pace the right atrium. In a second embodiment (FIG. 4b), an electrode resides in the right ventricle to add right ventricular pacing. As will be described, the '061 patent describes an oppositely polarized electrode (which may be exposed on a subcutaneously placed implantable pulse generator).
It is Applicants' understanding the design of the '061 patent has not enjoyed great commercial success. Applicants believe this is due, at least in part, to the separate development of smaller profile leads and more reliable atrial attachment techniques. Both of these developments address the problems of dual chamber pacing otherwise addressed by the '061 patent.
b. Pacing for Congestive Heart Failure
Beginning in the 1990's, cardiac pacing has been considered for treatment of congestive heart failure (CHF). CHF patients suffer from low left ventricular output.
CHF is an extremely serious and progressive disease. While drug treatments exist, they may delay but do not stop or reverse the disease.
CHF patients face a progression of a debilitating condition which drastically alters lifestyle and will ultimately be fatal in the absence of heart transplant. Unfortunately, many patients do not qualify for such transplants and the available number of donor hearts is inadequate to treat those who do qualify.
Many CHF patients have low left ventricular output due to a mismatch between contractile forces produced by muscles of the left ventricle free wall (the external wall of the left ventricle) and the opposing septum (the wall dividing the right and left ventricles). Ideally, the free wall and septum contract in synchrony during systole to urge blood through the aortic valve. When out of synchrony, the septal wall may be contracting while the free wall is relaxed. Instead of urging blood flow, at least a portion of the contractile energy of the septum is wasted.
The mismatch of free wall and septal contractility is believed to be due to disorders in the electrical conduction systems of the heart. This conduction system includes the A-V node, the Bundle of His and the Purkinje fibers.
Located at the upper end of the septum, the sinus node creates the synchronized neuraly-mediated signal for cardiac pacing. These signals are conducted by the specialized fibers comprising the A-V node and the Bundle of His (extending along the length of the septum) and further conducted to the muscle of the heart through the Purkinje fibers. The Purkinje fibers originate in the septum and extend through the apex of the heart and to the exterior walls of the heart including into and up the free wall of the left ventricle.
In a healthy heart, the signal flow from the A-V node to the free wall of the left ventricle is rapid to insure the free wall and septum contract in synchrony. For example, a stimulating signal may flow to the free wall in about 70-90 milli-seconds. In patients with conduction abnormalities, this timing may be significantly delayed (to 150 milli-seconds or more) resulting in asynchronous contraction.
In some patients, the conduction path through the Purkinje fibers may be blocked. The location of the block may be highly localized (as in the case of so-called “left bundle branch block” or LBBB) or may include an enlarged area of dysfunctional tissue (which can result from infarction). In such cases, all or a portion of the free wall of the left ventricle is flaccid while the septum is contracting. In addition to contributing to asynchronous contraction, the contraction force of the free wall is weakened.
To address asynchronous contraction, CHF patients can be treated with cardiac pacing of the left ventricle. Such pacing includes applying a stimulus to the septal muscles in synchrony with stimulation applied to the muscles of the free wall of the left ventricle. While infracted tissue will not respond to such stimulus, non-infarcted tissue will contract thereby heightening the output of the left ventricle.
The prior art has developed various techniques for accomplishing left ventricle stimulation. For reasons noted above (i.e., emboli formation), endocardially positioned electrodes in the left ventricle are avoided. However, electrodes can be placed on the epicardial surface of the heart through surgical placement. The epicardial electrodes are positioned on the free wall of the left ventricle and are paced in synchrony with electrodes placed near the septum in the right ventricle.
Since epicardial electrodes require a surgical placement, the patient is subjected to two procedures—percutaneous placement of right ventricle electrodes (normally performed in a catheter lab by an electrophysiologist) and surgical placement of epicardial electrodes on the left ventricle (normally placed by a cardiac surgeon in a surgical suite). Also, such dual procedure is a burden on medical resources.
Percutaneous procedures have been developed for placement of an electrode to stimulate the free wall of the left ventricle. In such a procedure, an electrode lead is advanced through the coronary sinus. Part of the venous system, the coronary sinus extends from the right atrium and wraps around the heart on or near the epicardial surface and partially overlies the left ventricle free wall. In this percutaneous procedure, the electrode remains positioned in the coronary sinus overlying the left ventricle free wall with the lead passing through the coronary sinus and through the right atrium to the implantable pulse generator.
Unfortunately, a coronary sinus electrode is frequently less than optimal. The portion of the free wall most directly influenced by the electrode is the tissue directly underlying the coronary sinus at the location of the electrode. For many patients, this may not be the location of the free wall most in need of a stimulating therapy. Accordingly, the resulting therapy is sub-optimal. Also, some patients may have an extremely small diameter coronary sinus or the coronary sinus may have such a tortuous shape that percutaneous positioning of an electrode within the coronary sinus is impossible or very difficult. Not uncommonly, advancing a lead from the right atrium into the coronary sinus is extremely time-consuming. Even if successful, such a procedure consumes significant health care resources (including precious catheter lab time). Finally, there are now up to three leads passing through and occupying the space of the superior vena cava (i.e., leads for the electrodes in the right ventricle, right atrium and the coronary sinus). U.S. patent application Publ. No. 2005/0125041 published Jun. 9, 2005 shows (in FIG. 1) three leads passed through a superior vena cava with one lead residing in the right atrium, one in the right ventricle and one passed through the coronary sinus to overly the left ventricle.
Attempts at pacing the left ventricle by pacing stimulation in the right ventricle have been suggested. U.S. Pat. No. 6,643,546 B2 to Mathis et al. dated Nov. 4, 2003 describes a lead with an array of electrodes along its length. The lead is placed in the right atrium and extending through the right ventricle, along the septal wall, and into the pulmonary artery. The concept requires that multiple electrodes from the array be pulsed simultaneously at significantly high voltages to produce an adequate electrical field to stimulate the LV septum. The current output from the pulse generator and battery will be very high due to the multiplicity of electrodes and high pacing voltages. Such high output will cause a clinically unacceptable product lifespan. Since a large number of electrodes and supporting electronics are needed to implement such a therapy delivery mechanism, it is not known yet whether it is practically feasible, not least to mention that it is very complicated both in terms of device design/manufacturing as well clinical practice. No published reports known to this date have demonstrated the functional as well as clinical benefits for this multiple electrode stimulation approach in the ventricle.
As will be described with reference to a preferred embodiment, the present invention is directed to a left ventricle pacing system and method which does not require epicardial electrodes or electrodes in a coronary sinus. As will be described, the present invention includes electrodes in the right ventricle near the septal wall. These electrodes create a pulsed electrical field which stimulates both the septum and at least a portion of the free wall of the left ventricle. The present invention achieves these objectives without requiring excessive energy demands or power consumption.